Abstract

The occurrence of vancomycin-resistant enterococci (VRE) continues to be an escalating problem throughout the world [ 1, 2]. The risk of VRE infection is greatest for elderly persons and severely ill patients who have been treated with extensive courses of antibiotics [2] and who are maintained in facilities (intensive care units [ICU] or transplant wards) where the incidence of VRE is high. In this regard, a recent study by Streit et al [1] determined that ~28°/o of all enterococci isolated from ICU patients in Canada and the United States were vancomycin resistant. The first reports of VRE appeared in the mid-1980s and included patients from both Europe and the United States [3]. More recent analyses of the specific enterococci involved in this resistance reveal that the predominant form of VRE identified in ICUs was R faecium (almost 70%), whereas R faecaliswas less common (~10°/o) [4], Furthermore, it appears that the incidence of vancomycin-resistant E. faecium is on the rise [5]. As the percentage of positive isolates of vancomycinresistant E. faecium becomes more prevalent, it is clear that, although our overall understanding of the pathogenesis of £. faecium is very limited [6], knowledge on this topic is becoming a high priority. The spread of E. faecium occurs primarily though hospital nosocomial infections. R faecium is commonly associated with ICU patients who are receiving antibiotic treatment [7], and most strains are resistant to multiple classes of antibiotics [8]. In addition, as the incidence of VRE increases, so does the rate of coinfection with methicillin-resistant Staphylococcus aureus (MRSA) [9, 10]. This coinfection profile appears to have led to the transfer of vancomycin resistance to MRSA. Although the occurrence is relatively small, several multidrug-resistant S. aureus strains have been isolated [11-13]. Recently, patients with heteroresistant vancomycin-intermediate S. aureus (hVISA) infection were evaluated and compared with MRSA-infected patients [13], and it was found that the hVISA-infected patients exhibited an extended duration of bacteremia with higher rates of complications [ 14] . Although few of the patients diagnosed with hVISA infection survived after receiving various treatments, most of these patients had additional health issues that likely contributed to their deaths. In this issue of the Journal Leenderste et al [15] describe provocative data suggesting that a concurrent E. faecium VRE load arising from the intestine can confine polymicrobial peritonitis and attenuate the inflammatory response in a murine model system. The authors evaluated the effect of this clinically relevant organism associated with nosocomial infections by using a hospital isolate that belongs to a genetic subpopulation that is widely found in hospitals namely, VRE strain E155. Although the mice used in the present study experienced VRE colonization from gastric inoculation, the mice presented with no infections at other sites until cecal

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